Among the most striking examples of adaptive parasite responses to the host environment is the impact of larval trematode infections on the reproductive biology of the molluscan intermediate host. In the majority of cases, larval infection leads to a complete cessation of host egg production, often referred to as parasitic castration. For trematode species which utilize only "nonfeeding" sporocyst stages in their intramolluscan development, reproductive inhibition is believed to be chemically-mediated, involving the secretion of molecules that have either direct or indirect effects on the gonads or accessory sex organs. Recent evidence in the avian schistosome-snail (Trichobilharzia-Lymnaea) system strongly suggests that the initial phases of host castration involve larval disruption of several neuroendocrine pathways. However, the specific mechanisms underlying this disruptive influence is not yet known. In the current application, Schistosoma mansoni and Biomphalaria glabrata will be employed as a parasite-host model to investigate the molecular mechanisms underlying trematode-mediated castration. Emphasis will be placed on the interaction of larvae and the host endocrine system in initiating suppression of reproductive function. It is anticipated that the results of these studies will contribute greatly to our basic understanding of hormonal regulation of host reproduction and how parasites effectively modulate this process. Ultimately such information may have potential application to control of schistosomiasis transmission through the chemically-mediated control of reproductive activity in the snail vector.